Studies are continuing to examine molecular mechanisms by which species of oral actinomycetes adhere to other plaque bacteria and to mammalian cells. Lectin sites which are inhibited by lactose are associated with the surface fimbriae (i.e. pili) of many human strains of Actinomyces viscosus and A. naeslundii. These sites mediate coaggregation of the actinomycetes with certain oral streptococci and hemagglutination of the actinomycetes with neuraminidase-treated human erythrocytes. Thus, interactions of a lectin-carbohydrate type may contribute significantly to the distribution of certain bacteria within the oral cavity.